Search Results (657)

Lower respiratory tract infections caused by Pseudomonas aeruginosa are a global concern. Patients with chronic lung diseases such as cystic fibrosis and non-cystic fibrosis bronchiectasis often do not receive adequate antibiotic delivery through conventional routes. P. aeruginosa employs several mechanisms, including biofilm formation and efflux pumps to limit the accumulation of bactericidal drug concentrations. Direct drug delivery to the lung epithelial lining fluid can increase antibiotic concentration and reduce treatment failure rates. This review discusses current research and developments in inhaled antibiotic formulations for treating P. aeruginosa infections. Recent studies on particle engineering for the dry powder inhalers of antibiotics emphasized three fundamental principles of development: micro, nano, and nano-in-microparticles. Carrier-free microparticles showed potential for high-dose delivery but suffered from poor aerosolization, which could be improved through a drug–drug combination. Amino acids in a co-spray-dried system improved powders’ aerodynamics and reduced moisture sensitivity while incorporating the chitosan/poly(lactic-co-glycolic acid) (PLGA)-modified release of the drug. Nano-in-microsystems, embedding lipid carriers, showed improved antibiofilm activity and controlled release. We also highlight emerging biologics, including antibacterial proteins/peptides, vaccines, bacteriophages, and probiotics. Research on antibiotics and biologics for inhalation suggests excellent safety profiles and encouraging efficacy for some formulations, including antimicrobial peptides and bacteriophage formulations. Further research on novel molecules and synergistic biologic combinations, supported by comprehensive animal lung safety investigations, will be required in future developments. Full article

Purpose: Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory condition often accompanied by various comorbidities that significantly affect patient outcomes. High resolution computed tomography (HRCT) has emerged as a valuable tool for diagnosing and managing COPD-related comorbidities. This study aimed to explore the impact of chest computed tomography (CT) imaging in identifying and characterizing comorbidities in COPD patients. Methods: The study was conducted on 99 patients with COPD, the median age of the study population was 70.0 years (Q1–Q3: 62.0–75.0); 86% were men (85), and 14% were women (14). All patients underwent chest HRCT to identify the presence of comorbidities. Results: According to the GOLD classification (ABE groups), 3% were type A, 27% were type B, and 69% were type E. The prevalence of comorbidities identified on chest HRCT was reported as 66% for coronary artery calcification (CAC), 83% for osteoporosis, 36% for pulmonary artery enlargement (PAE), 31% for emphysema, 19% for bronchiectasis, 17% for hiatal hernia, 14% for lung cancer, 12% pulmonary infections, and 3% for interstitial abnormalities. In 4%, there were no comorbidities, one comorbidity was found in 11%, two comorbidities in 17%, and three comorbidities and more in 68% of cases. Conclusions: Chest HRCT imaging serves as a valuable tool for identifying and assessing comorbidities in patients with COPD. Incorporating chest CT imaging into the routine evaluation of COPD patients may contribute to a more comprehensive understanding of their condition and lead to better clinical outcomes. Full article

Background: Sex-based disparities in the presentation, management, and outcomes of infective endocarditis (IE) remain insufficiently characterized despite their growing recognition. This study systematically evaluates current evidence on sex differences in the presentation, treatment, and outcomes of IE. Methods: A systematic review and meta-analysis were conducted according to PRISMA and Cochrane guidelines. EMBASE, MEDLINE, PubMed, the Cochrane Library, and Google Scholar were searched up to October 2024. Twenty-four studies including 139,952 patients (79,698 men and 60,254 women) were analyzed. Primary outcomes were mortality (in-hospital, 30-day, and 1-year), stroke, and treatment modality (medical vs. surgical). Secondary outcomes included complications, procedural characteristics, and hospital course. Results: Men were younger at diagnosis and had higher rates of substance abuse and coronary artery disease, while women more often had hypertension, diabetes, chronic lung disease, and prior valvular pathology. Men more frequently had aortic and prosthetic valve IE, whereas women had mitral and tricuspid involvement. Men were about 65% more likely to undergo surgery for infective endocarditis than women, while women were predominantly managed medically. Men had lower in-hospital (OR 0.81, 95% CI 0.72–0.92) and 1-year mortality (OR 0.76, 95% CI 0.61–0.94), though 30-day mortality did not differ significantly. Women experienced shorter hospital stays but longer ICU admissions and more heart failure, whereas men had more recurrent IE. Conclusions: Men underwent surgery more often and had better short- and long-term survival. Women presented later, with greater comorbidity and higher complication rates. Enhanced recognition of sex-specific risk and equitable surgical referral may improve IE outcomes. Full article

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with uncertain etiology. Chronic viral infection, including Epstein–Barr virus (EBV), has been implicated as a potential driver of repetitive epithelial injury and dysregulated repair. We sought to evaluate and define the breadth versus specificity of EBV-directed humoral immunity in IPF. We performed proteome-scale serological profiling using an EBV protein microarray (202 proteins) representing all proteins expressed by the EBV proteome (type I and II) on plasma samples from 32 patients with confirmed IPF (87.5% male; mean age 60.9 years) and 15 healthy disease-free controls (40% male; mean age 57.9 years). Per-sample global EBV IgG means were higher in IPF than controls (Welch p = 0.005), and the difference persisted after sex adjustment (p = 0.012). Although no single antigen met a stringent FDR significance threshold, 10 EBV antigen-specific antibody responses showed nominal elevation in IPF, with 2 remaining nominally significant after sex adjustment and 5 additional antibody responses reaching significance only in linear regression models. Overall, these results support the concept that IPF is associated with a diffuse elevation of EBV-directed humoral responses rather than antigen-specific dominance, consistent with ongoing, low-level viral reactivation. The presence of an EBV-negative subgroup within the IPF cohort underscores etiological heterogeneity within IPF. Full article

Background/Objective: Pulmonary impairments have been identified as some of the most complex and debilitating post-acute sequelae of SARS-CoV-2 infection (PASC) or long COVID. This study identified and characterised the specific forms of pulmonary impairments detected using pulmonary function tests (PFT), chest X-rays (CXR), and computed tomography (CT) scans in patients with long COVID symptoms. Methods: We conducted a single-centre retrospective study to evaluate 60 patients with long COVID who underwent PFT, CXR, and CT scans. Pulmonary function in long COVID patients was assessed using defined thresholds for key test parameters, enabling categorisation into normal, restrictive, obstructive, and mixed lung-function patterns. We applied exact binomial (Clopper–Pearson) 95% confidence intervals to calculate the proportions of patients falling below the defined thresholds. We also assessed the relationships among spirometric indices, lung volumes, and diffusion capacity (DLCO) using scatter plots and corresponding linear regressions. The findings from the CXRs and CT scans were categorised, and their prevalence was calculated. Results: A total of 60 patients with long COVID symptoms (mean age 60 ± 13 years; 57% female) were evaluated. The cohort was ethnically diverse and predominantly non-smokers, with a mean BMI of 32.4 ± 6.3 kg/m². PFT revealed that most patients had preserved spirometry, with mean Forced Expiratory Volume in 1 Second (FEV1) and Forced Vital Capacity (FVC) above 90% predicted. However, a significant proportion exhibited reductions in lung volumes, with total lung capacity (TLC) decreasing in 35%, and diffusion capacity (DLCO/TLCO) decreasing in 75%. Lung function pattern analysis showed 88% of patients had normal function, while 12% displayed a restrictive pattern; no obstructive or mixed patterns were observed. Radiographic assessment revealed that 58% of chest X-rays were normal, whereas CT scans showed ground-glass opacities (GGO) in 65% of patients and fibrotic changes in 55%, along with findings such as atelectasis, air trapping, and bronchial wall thickening. Conclusions: Spirometry alone is insufficient to detect impairment of gas exchange or underlying histopathological changes in patients with long COVID. Our findings show that, despite normal spirometry results, many patients exhibit significant diffusion impairment, fibrotic alterations, and ground-glass opacities, indicating persistent lung and microvascular damage. These results underscore the importance of comprehensive assessment using multiple diagnostic tools to identify and manage chronic pulmonary dysfunction in long COVID. Full article

Antibiotic-resistant infections remain a major challenge in cystic fibrosis (CF), where chronic Pseudomonas aeruginosa colonization drives lung infection. The overexpression of adhesion-related proteins and extracellular matrix components, including fibronectin (Fn), facilitates bacterial colonization. Recent evidence identifies the RNA-binding protein Human Antigen R (HuR) as a key regulator of this process, as it stabilizes Vav3 mRNA, promoting Fn deposition and the formation of bacterial docking platforms. Here, we report the synthesis, optimization, and functional evaluation of the HuR-targeted small-molecule (2S,3S)-BOPC1. Functional assays in CF human airway epithelial cells demonstrated that (2S,3S)-BOPC1 significantly reduced P. aeruginosa adhesion in a dose-dependent manner without detectable cytotoxic effects. These findings provide the first evidence that targeting HuR can disrupt the HuR–Vav3–Fn axis, reducing bacterial attachment. This host-directed approach represents a promising strategy to prevent chronic infections in CF without promoting antibiotic resistance. Full article

Background and Objectives: COVID-19 is an infection caused by the SARS-CoV-2 coronavirus that may develop several complications. Interstitial lung disease (ILD) is the major long-term complication of COVID-19 disease leading to progressive lung fibrosis and reduced respiratory function. The aim of this narrative review is to provide an updated overview of post-COVID-19 ILD by examining research publications and clinical guidelines selected from PubMed, Web of Science, and major respiratory medicine journals from 2020 to 2025. Methods: ILDs are diagnosed by medical history, physiological examination, pulmonary function tests, and chest X-ray or high-resolution computed tomography (HRCT) scan. Lung biopsy, especially cryobiopsy or video-assisted thoracoscopic (VATS) biopsy, can be performed to define histological patterns and confirm the diagnosis. Results: Post-COVID-19 ILD is a chronic condition characterized by long-term respiratory symptoms, radiological findings, and reduced lung function. Fibrotic injury is a consequence of the initial infection and could be influenced by persistent inflammation and dysregulated tissue repair. Risk factors include severe acute illness, advanced age, male sex, and smoking. Clinical course and prognosis of post-COVID-19 ILD is uncertain, as most patients experience gradual improvement or stability, whereas others develop progressive lung function decline. Treatment of post-COVID-19 ILD is not presently defined by guidelines but comprises corticosteroids, antifibrotics (including new drugs such as nerandomilast), supportive oxygen, pulmonary physiotherapy rehabilitation, smoking cessation, and vaccination. Conclusions: ILD represents a significant long-term complication of COVID-19 infection. Further investigations are required to better understand its pathophysiology and clinical management. As research progresses, more effective diagnostic and therapeutic strategies are expected to emerge. Full article

West Nile virus (WNV) is an arthropod-borne flavivirus first identified in 1937. Over time, WNV has spread globally and is now endemic in Italy. Although most human WNV infections are asymptomatic (80%), less than 1% progress to a neuroinvasive disease with high mortality rates. This case involves a 45-year-old woman with post-surgical hypoparathyroidism and Sjögren’s syndrome who developed severe encephalomyelitis linked to WNV, leading to ventilator-associated pneumonia and death. Neuropathological findings revealed a bilaterally cribriform thalamus and reddish punctate lesions near the dentate nucleus of the cerebellum. The trachea and bronchial hilum branches contained whitish foamy liquid. The left lung showed multiple brownish-violet areas, with whitish regions at dissection. The heart appeared unremarkable. A detailed neuropathological examination focused on areas involved in motor control pathways. Tissue samples were stained with hematoxylin and eosin and trichrome techniques, and immunohistochemistry was performed using CD68, CD3, and CD20. A significant damage was observed in the lenticular nucleus and motor thalamus, with prominent concentric vascular calcifications. The cerebellar cortex showed near-total depletion of Purkinje cells. In the spinal cord, CD68 and CD3 positivity was noted in the lateral funiculi, anterior horns, and Clarke’s column. Lung findings showed pulmonary edema, chronic emphysema, and bronchopneumonia. The observed CD3 and CD68 positivity confirms that WNV spreads trans-synaptically along motor control pathways. We speculate on the potential molecular mechanisms by which hypoparathyroidism and Sjögren’s syndrome may have played a role in the neuroinvasive progression of the disease. Full article

N6-methyladenosine (m⁶A) represents the most abundant and tightly controlled modification within eukaryotic mRNA, critically influencing RNA metabolism and function. The m⁶A methyltransferase Like-3 (METTL3), responsible for the complex’s catalytic function, has emerged as a central epitranscriptomic regulator governing mRNA stability, alternative splicing, nuclear export, and the efficiency of mRNA translation. Converging research shows that METTL3 is involved in the pathogenesis of numerous disorders via m⁶A-dependent, post-transcriptional regulation of gene programs controlling cell growth, migration, and immune pathways. Regarding pulmonary pathophysiology, METTL3-mediated m⁶A is tied to disease initiation and progression in conditions such as asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), lung infections, acute respiratory distress syndrome (ARDS). This review summarizes the contemporary evidence for METTL3’s roles and regulatory network in diverse pulmonary pathologies. We further highlight emerging strategies for targeting METTL3 as a potential therapeutic approach, underscoring its promise as a novel epitranscriptomic target. Beyond inflammatory and fibrotic disorders, we also summarize emerging evidence linking METTL3 to lung cancer and briefly outline other respiratory conditions (e.g., ILD, bronchiectasis, and secondary pulmonary hypertension), highlighting common translational themes and remaining gaps. Further studies are required to clarify the disease-specific and context-dependent actions of METTL3 and to advance the clinical translation of m⁶A-based therapies. Full article

Background/Objectives: Quantitative computed tomography (CT) metrics are widely used to assess pulmonary involvement and to predict short-term severity in coronavirus disease 2019 (COVID-19). However, it remains unclear whether baseline artificial intelligence (AI)-based quantitative high-resolution computed tomography (HRCT) metrics of pneumonia burden provide incremental prognostic value for in-hospital composite adverse outcomes beyond routine clinical factors, or whether these imaging-derived markers carry any exploratory signal for long-term severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reinfection among hospitalized patients. Most existing imaging studies have focused on diagnosis and acute-phase prognosis, leaving a specific knowledge gap regarding AI-based quantitative HRCT correlates of early deterioration and subsequent reinfection in this population. To evaluate whether combining deep learning-derived, quantitative, HRCT features and clinical factors improve prediction of in-hospital composite adverse events and to explore their association with long-term reinfection in patients with COVID-19 pneumonia. Methods: In this single-center retrospective study, we analyzed 236 reverse-transcription polymerase chain reaction (RT-PCR)-confirmed COVID-19 patients who underwent baseline HRCT. Median follow-up durations were 7.65 days for in-hospital outcomes and 611 days for long-term outcomes. A pre-trained, adaptive, artificial-intelligence-based, prototype model (Siemens Healthineers) was used for pneumonia analysis. Inflammatory lung lesions were automatically segmented, and multiple quantitative metrics were extracted, including opacity score, volume and percentage of opacities and high-attenuation opacities, and mean Hounsfield units (HU) of the total lung and opacity. Patients were stratified based on receiver operating characteristic (ROC)-derived optimal thresholds, and multivariable Cox regression was used to identify predictors of the composite adverse outcome (intensive care unit [ICU] admission or all-cause death) and SARS-CoV-2 reinfection, defined as a second RT-PCR-confirmed episode of COVID-19 occurring ≥90 days after initial infection. Results: The composite adverse outcome occurred in 38 of 236 patients (16.1%). Higher AI-derived opacity burden was significantly associated with poorer outcomes; for example, opacity score cut-off of 5.5 yielded an area under the ROC curve (AUC) of 0.71 (95% confidence interval [CI] 0.62–0.79), and similar performance was observed for the volume and percentage of opacities and high-attenuation opacities (AUCs up to 0.71; all p < 0.05). After adjustment for age and comorbidities, selected HRCT metrics—including opacity score, percentage of opacities, and mean HU of the total lung (cut-off −662.38 HU; AUC 0.64, 95% CI 0.54–0.74)—remained independently associated with adverse events. Individual predictors demonstrated modest discriminatory ability, with C-indices of 0.59 for age, 0.57 for chronic obstructive pulmonary disease (COPD), 0.62 for opacity score, 0.63 for percentage of opacities, and 0.63 for mean total-lung HU, whereas a combined model integrating clinical and imaging variables improved prediction performance (C-index = 0.68, 95% CI: 0.57–0.80). During long-term follow-up, RT-PCR–confirmed reinfection occurred in 18 of 193 patients (9.3%). Higher baseline CT-derived metrics—particularly opacity score and both volume and percentage of high-attenuation opacities (percentage cut-off = 4.94%, AUC 0.69, 95% CI 0.60–0.79)—showed exploratory associations with SARS-CoV-2 reinfection. However, this analysis was constrained by the very small number of events (n = 18) and wide confidence intervals, indicating substantial statistical uncertainty. In this context, individual predictors again showed only modest C-indices (e.g., 0.62 for procalcitonin [PCT], 0.66 for opacity score, 0.66 for the volume and 0.64 for the percentage of high-attenuation opacities), whereas the combined model achieved an apparent C-index of 0.73 (95% CI 0.64–0.83), suggesting moderate discrimination in this underpowered exploratory reinfection sample that requires confirmation in external cohorts. Conclusions: Fully automated, deep learning-derived, quantitative HRCT parameters provide useful prognostic information for early in-hospital deterioration beyond routine clinical factors and offer preliminary, hypothesis-generating insights into long-term reinfection risk. The reinfection-related findings, however, require external validation and should be interpreted with caution given the small number of events and limited precision. In both settings, combining AI-based imaging and clinical variables yields better risk stratification than either modality alone. Full article

Chronic infections pose significant clinical challenges due to their persistent nature, heightened resistance to conventional therapies, and association with biofilm formation. Neutrophil extracellular traps (NETs), released through a unique form of cell death known as NETosis, serve as an innate immune defense mechanism by trapping and neutralizing pathogens. However, accumulating evidence reveals a complex and paradoxical relationship between NETs and microbial biofilms. While NETs can immobilize and kill planktonic microbes, the extracellular DNA and associated proteins often contribute to biofilm stability, immune evasion, and chronic infection persistence. This review explores the bidirectional interactions between NETosis and biofilm formation, with a focus on their synergistic roles in the pathogenesis of chronic infections such as cystic fibrosis lung disease, diabetic foot ulcers, periodontitis, and implant-associated infections. We outline the molecular mechanisms governing NETosis, the structural and functional dynamics of biofilms, and how these processes intersect to form recalcitrant infection niches. Emerging therapeutic strategies aimed at disrupting this pathogenic interplay including DNase-based treatments, PAD4 inhibitors, and combination therapies are critically evaluated. By illuminating the pathogenic synergy between NETs and biofilms, this review underscores the need for integrated immunomodulatory and anti-biofilm interventions to effectively manage chronic infectious diseases and improve patient outcomes. Full article

Background: Non-cystic fibrosis bronchiectasis (BE) is a chronic lung condition characterized by irreversible bronchial dilation and presented with persistent respiratory symptoms, recurrent respiratory infections, and decreased quality of life. Inhaled corticosteroids (ICSs) are frequently prescribed in patients with bronchiectasis, despite limited evidence supporting their clinical efficacy. Inhaled corticosteroids have been associated with increased risk of respiratory infection with Haemophilus influenzae (H. influenzae) in other groups of lung diseases. We aimed to evaluate the association between ICS use and the risk of isolating H. influenzae from lower respiratory tract samples in patients with bronchiectasis. Methods: A retrospective cohort study was conducted using data from 2010 to 2018, encompassing all patients diagnosed with bronchiectasis in outpatient clinics in Eastern Denmark. ICS use was standardized in budesonide equivalent doses and categorized in tertiles: low (<210 μg/day), moderate (211–625 μg/day), and high (≥626 μg/day) based on cumulative budesonide equivalent doses redeemed in the 12 months before cohort entry. The primary outcome was the first isolation of H. influenzae from lower respiratory tract samples post-cohort entry. Cox proportional hazards models, adjusted for relevant confounders, estimated hazard ratios (HRs), and inverse probability-of-treatment weighting (IPTW) was used in sensitivity analyses. Results: Among 3663 patients (mean age 66 years; 61% female), 2175 (59.4%) did not use ICS, while 484 (13.2%), 508 (13.9%), and 496 (13.5%) were in the low-, moderate-, and high-dose ICS groups, respectively. Furthermore, 594 (16.22%) patients had a lower respiratory tract culture positive for H. influenzae during follow-up. High-dose ICS use was associated with an increased risk of H. influenzae; HR 1.63 (95% Cl, 1.19 to 2.12, p < 0.005) compared with no ICS use. No association for low or moderate ICS use was found: low-dose ICS HR 0.75 (95% Cl, 0.52 to 1.07, p = 0.11) and moderate-dose ICS HR 1.27 (95% Cl, 0.93 to 1.72, p = 0.12). IPTW analysis confirmed the main finding. Conclusions: High-dose ICS use in patients with bronchiectasis was associated with an increased risk of acquiring H. influenzae in the lower respiratory tract. Hence, patients with bronchiectasis should be cautiously prescribed high-dose ICS. Full article

Introduction: Chest drainage is central to thoracic surgery, pleural medicine, and emergency care, yet practice remains heterogeneous in tube caliber, access, suction, device selection, and removal thresholds. This narrative review aims to synthesize evidence and translate it into guidance. Materials and Methods: We performed a narrative review with PRISMA-modeled transparency. Using backward citation from recent comprehensive overviews, we included randomized trials, meta-analyses, guidelines/consensus statements, and high-quality observational studies. We extracted data on indications, technique, tube size, analog versus digital drainage, suction versus water-seal drainage, removal criteria, and key pleural conditions. Due to heterogeneity in device generations, suction targets, and outcomes, we synthesized the findings qualitatively according to converged evidence. Results: After lung resection, single-drain strategies, early use of water-seal, and standardized removal at ≤300–500 mL/day reduce pain and length of stay without increasing the need for reintervention; digital systems support objective removal using sustained low-flow thresholds (approximately 20–40 mL/min). Small-bore (≤14 Fr) Seldinger catheters perform comparably to larger tubes for secondary and primary pneumothorax and enable ambulatory pathways. In trauma, small-bore approaches can match large-bore drainage in stable patients when paired with surveillance and early escalation of care. For pleural infection, image-guided drainage, combined with fibrinolytics or surgery, is key. Indwelling pleural catheters provide relief comparable to talc in dyspnea associated with malignant effusions in patients with non-expandable lungs. Complications are mitigated by ultrasound guidance and avoiding abrupt high suction after chronic collapse; however, these strategies must be balanced against risks of malposition, occlusion or retained collections, prolonged air leaks, and device complexity, which demand protocolized escalation and team training. Conclusions: Practice coalesces around three pillars—right tube, right system, proper criteria. Adopt standardized pathways, device-agnostic thresholds, and volume or airflow criteria. Trials should harmonize “seal” definitions and validate telemetry-informed removal strategies. Full article

Background/Objective: The SARS-CoV-2 pandemic, emerging in late 2019, led to a global health crisis, with many patients developing prolonged symptoms after infection known as sequelae of COVID-19. This condition is theorized to be driven by systemic inflammation and immune dysregulation and presents with diverse symptoms from cardiovascular, pulmonary, and neurological systems. This study investigates the prevalence, risk factors, and long-term impacts of sequelae of COVID-19. Method: Using Denmark’s healthcare databases, this population-based cohort study included 1,034,093 individuals over 40 years who tested positive for COVID-19 between 1 March 2020 and 28 February 2022. Participants were divided into two age groups: 40–59 years and 60 years or older. Part A examined the risk of sequelae of COVID-19 diagnoses (ICD-10 code B94.8A) based on the Charlson Comorbidity Index (CCI). Part B assessed two-year outcomes for patients diagnosed with sequelae of COVID-19. Results: Results showed a 0.55% prevalence of sequelae of COVID-19 in both age groups. Higher CCI scores correlated with an increased risk of sequelae of COVID-19. During the two-year follow-up, patients with sequelae of COVID-19 faced significantly elevated risks of thromboembolic events, chronic lung diseases, and infections. Adjusted hazard ratios were notably high: 14.50 (7.54–27.86) and 12.50 (6.95–22.49) for thromboembolic events in adults and older adults, respectively; 33.81 (13.30–85.96) and 9.83 (6.09–15.87) for chronic lung disease; and 8.40 (4.49–15.70) and 15.44 (10.47–22.78) for infections. Conclusions: While the overall prevalence of sequelae of COVID-19 was low among individuals over 40, those with higher comorbidity burdens were at greater risk of severe sequelae and subsequent health complications. These findings underscore the need for clinical monitoring, especially for patients with pre-existing comorbidities, to mitigate long-term health risks associated with COVID-19 sequelae. Full article

This review focuses on the diverse etiologies of secondary spontaneous pneumothorax (SSP) and the crucial role of imaging in their diagnosis. Unlike primary spontaneous pneumothorax (PSP), which is typically due to ruptured blebs, SSP results from a wide array of underlying pulmonary conditions that can pose significant diagnostic challenges. These include infections like tuberculosis, airway diseases such as chronic obstructive pulmonary disease, malignancies (primary and metastatic), interstitial lung diseases like sarcoidosis, cystic lung diseases such as lymphangioleiomyomatosis, and connective tissue disorders. In women, catamenial pneumothorax secondary to endometriosis should be considered. The role of radiologists is crucial in uncovering these underlying conditions. While chest radiography is the initial imaging modality, computed tomography (CT) provides superior sensitivity for detecting subtle parenchymal abnormalities. Advanced techniques like photon-counting detector CT offer further benefits, including enhanced spatial resolution, reduced noise, and lower radiation dose, potentially revealing underlying causes that might be missed with conventional CT. This enhanced visualization of subtle parenchymal changes, small airways, and vascular structures can be the key to diagnosing the underlying cause of pneumothorax. Recognizing the diverse etiologies of SSP and utilizing advanced imaging techniques is paramount for accurate diagnosis, appropriate management, and improved patient outcomes. Full article